Dendritic Spine Loss and Synaptic Alterations in Alzheimer’s Disease DOI
Marlen Knobloch, Isabelle M. Mansuy

Molecular Neurobiology, Journal Year: 2008, Volume and Issue: 37(1), P. 73 - 82

Published: Feb. 1, 2008

Language: Английский

The Physiology, Signaling, and Pharmacology of Dopamine Receptors DOI
Jean‐Martin Beaulieu, Raul R. Gainetdinov

Pharmacological Reviews, Journal Year: 2011, Volume and Issue: 63(1), P. 182 - 217

Published: Feb. 8, 2011

G protein-coupled dopamine receptors (D1, D2, D3, D4, and D5) mediate all of the physiological functions catecholaminergic neurotransmitter dopamine, ranging from voluntary movement reward to hormonal regulation hypertension. Pharmacological agents targeting dopaminergic neurotransmission have been clinically used in management several neurological psychiatric disorders, including Parkinson9s disease, schizophrenia, bipolar disorder, Huntington9s attention deficit hyperactivity disorder (ADHD1), Tourette9s syndrome. Numerous advances occurred understanding general structural, biochemical, functional properties that led development multiple pharmacologically active compounds directly target receptors, such as antiparkinson drugs antipsychotics. Recent progress complex biology receptor-related signal transduction mechanisms has revealed that, addition their primary action on cAMP-mediated signaling, can act through diverse signaling involve alternative protein coupling or protein-independent via interactions with ion channels proteins are characteristically implicated receptor desensitization, β-arrestins. One future directions managing dopamine-related pathologic conditions may a transition approaches affect function precise postreceptor intracellular modalities either ligand-biased pharmacology. In this comprehensive review, we discuss classification, basic structural genetic organization, distribution brain periphery, mechanisms. addition, abnormalities expression, function, documented human disorders current pharmacology emerging trends novel therapeutic at and/or related events.

Language: Английский

Citations

2488
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms DOI Open Access
Ami Citri, Robert C. Malenka

Neuropsychopharmacology, Journal Year: 2007, Volume and Issue: 33(1), P. 18 - 41

Published: Aug. 29, 2007

Language: Английский

Citations

1937
Glycogen synthase kinase-3 (GSK3): Regulation, actions, and diseases DOI
Eléonore Beurel, Steven F. Grieco,

Richard S. Jope

et al.

Pharmacology & Therapeutics, Journal Year: 2014, Volume and Issue: 148, P. 114 - 131

Published: Nov. 29, 2014

Language: Английский

Citations

1488
Brain insulin resistance in type 2 diabetes and Alzheimer disease: concepts and conundrums DOI
Steven E. Arnold, Zoe Arvanitakis, Shannon L. Macauley

et al.

Nature Reviews Neurology, Journal Year: 2018, Volume and Issue: 14(3), P. 168 - 181

Published: Jan. 29, 2018

Language: Английский

Citations

1194
The GSK3 hypothesis of Alzheimer’s disease DOI Creative Commons
Claudie Hooper, Richard Killick, Simon Lovestone

et al.

Journal of Neurochemistry, Journal Year: 2007, Volume and Issue: 104(6), P. 1433 - 1439

Published: Dec. 18, 2007

J. Neurochem. (2008) 104, 1433–1439. Abstract Glycogen synthase kinase 3 (GSK3) is a constitutively active, proline‐directed serine/threonine that plays part in number of physiological processes ranging from glycogen metabolism to gene transcription. GSK3 also pivotal and central role the pathogenesis both sporadic familial forms Alzheimer’s disease (AD), an observation has led us coin ‘GSK3 hypothesis AD’. According this hypothesis, over‐activity accounts for memory impairment, tau hyper‐phosphorylation, increased β‐amyloid production local plaque‐associated microglial‐mediated inflammatory responses; all which are hallmark characteristics AD. If our AD’ substantiated indeed causal mediator AD then inhibitors would provide novel avenue therapeutic intervention devastating disorder.

Language: Английский

Citations

1114
Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake DOI Creative Commons
Shaomin Li, Soyon Hong,

Nina E. Shepardson

et al.

Neuron, Journal Year: 2009, Volume and Issue: 62(6), P. 788 - 801

Published: June 1, 2009

Language: Английский

Citations

888
Long-term depression in the CNS DOI
Graham L. Collingridge, Stéphane Peineau, John G. Howland

et al.

Nature reviews. Neuroscience, Journal Year: 2010, Volume and Issue: 11(7), P. 459 - 473

Published: June 18, 2010

Language: Английский

Citations

860
The Many Faces of Tau DOI Creative Commons
Meaghan Morris, Sumihiro Maeda,

Keith Vossel

et al.

Neuron, Journal Year: 2011, Volume and Issue: 70(3), P. 410 - 426

Published: May 1, 2011

Language: Английский

Citations

849
Dopamine: Functions, Signaling, and Association with Neurological Diseases DOI
Marianne Klein, Daniella S. Battagello, Ariel R. Cardoso

et al.

Cellular and Molecular Neurobiology, Journal Year: 2018, Volume and Issue: 39(1), P. 31 - 59

Published: Nov. 16, 2018

Language: Английский

Citations

808
Molecular and electrophysiological evidence for net synaptic potentiation in wake and depression in sleep DOI
Vladyslav V. Vyazovskiy, Chiara Cirelli,

Martha Pfister‐Genskow

et al.

Nature Neuroscience, Journal Year: 2008, Volume and Issue: 11(2), P. 200 - 208

Published: Jan. 20, 2008

Language: Английский

Citations

798